Abstract
Otitis media (OM) is the most prevalent childhood disease in developed countries. Involvement of innate immunity mediated by Toll-like receptors (TLRs) in OM has been implicated primarily in cell lines and by association studies of innate immune gene polymorphisms with OM prevalence. However, the precise role of innate immunity in OM is incompletely understood. We review recent research that has advanced our understanding of how innate immunity in the middle ear is mediated by the interaction of pathogen molecules with receptors such as the TLRs, leading to the activation of adaptor molecules and production of proinflammatory cytokines. TLR genes and signaling molecules are upregulated in OM in a murine model. Deletion of several key innate immune genes results in persistent OM in mice, coupled with an inability to clear bacterial infection from the middle ear. It is concluded that an intact innate immune signaling system is critical to recovery from bacterial OM.
| Original language | English |
|---|---|
| Journal | Current Allergy and Asthma Reports |
| Volume | 11 |
| Issue number | 1 |
| Pages (from-to) | 78-84 |
| Number of pages | 7 |
| ISSN | 1529-7322 |
| DOIs | |
| Publication status | Published - 01.02.2011 |
Funding
Acknowledgments This work was supported by National Institutes of Health/National Institute on Deafness and Other Communication Disorders grants no. DC006279 (to Dr. Wasserman) and no. DC000129 (to Dr. Ryan), the VA Research Service (Dr. Ryan), and grant no. E37-2010 (to Dr. Leichtle) from the University of Lübeck, Germany. Disclosure Dr. Wasserman has served as a consultant for Genentech and Merck & Co., has been employed by the American Board of Allergy and Immunology, has received grant support from Merck & Co. and Schering-Plough, and has been paid for providing expert testimony by various law firms. Drs. Leichtle, Lai, Wollenberg, and Ryan reported no potential conflicts of interest relevant to this article.
